Here is the list of the most common conditions beginning with letter “G“:
- Gastric dumping syndrome
- Gaucher’s disease
- Genu varum
- Gestational Pemphigoid
- Giant cell arteritis
- Glioblastoma multiforme (GBM)
Galactorrhea or galactorrhoea is the spontaneous flow of milk from the breast, unassociated with childbirth or nursing. Contemporary Maternal-Newborn Nursing Care defines galactorrhea as “nipple discharge.”
It can be due to dysregulation of certain hormones or local causes such as excessive nipple stimulation. Hormonal causes most frequently associated with galactorrhea are hyperprolactinemia and thyroid conditions with elevated levels of TSH or TRH hormones.
Lactation requires the presence of estrogen, progesterone and prolactin, and the evaluation of galactorrhoea includes eliciting a history for various medications or foods (methyldopa, opiates, antipsychotics, as well as licorice) and for behavioral causes (stress, and breast and chest wall stimulation), as well as evaluation for pregnancy, pituitary adenomas (with overproduction of prolactin or compression of the pituitary stalk), and hypothyroidism. Adenomas of the anterior pituitary are most often prolactinomas. Overproduction of prolactin leads to cessation of menstrual periods and infertility, which may be a diagnostic clue. Galactorrhoea may also be caused by hormonal imbalances owing to birth control pills.
Galactorrhoea is also a side effect associated with the use of the second-generation H2 receptor antagonist Cimetidine (trade name: Tagamet). Galactorrhoea can be also caused by anti-psychotics that cause hyperprolactinemia by blocking dopamine receptors responsible for control of prolactin release. Of these, risperidone is the most notorious for causing this complication. Case reports suggest Proton Pump inhibitors have been shown to cause Galactorrhoea.
Galactocele is a cystic tumor containing milk or a milky substance that is usually located in the mammary glands. It is caused by a protein plug that blocks off the outlet. Galactoceles are benign and are not a cause for concern. Once lactation has ended the cyst will resolve on its own without intervention. A galactocele does not cause infection as the milk within is sterile and has no outlet for which to become contaminated. Attempts to drain the cyst are unsuccessful because the protein plug remains intact and milk production continues.
Galactokinase deficiency, also known as Galactosemia type 2 or GALK deficiency, is an autosomal recessive metabolic disorder marked by an accumulation of galactose and galactitol secondary to the decreased conversion of galactose to galactose-1-phosphate by galactokinase. The disorder is caused by mutations in the GALK1 gene, located on chromosome 17q24 (McKusick, Kniffin, 2006). Galactokinase catalyzes the first step of galactose phosphorylation in the Leloir pathway of intermediate metabolism. Galactokinase deficiency is one of the three inborn errors of metabolism that lead to hypergalactosemia. The disorder is inherited as an autosomal recessive trait. Unlike classic galactosemia, which is caused by deficiency of galactose-1-phosphate uridyltransferase, galactokinase deficiency does not present with severe manifestations in early infancy. Its major clinical symptom is the development of cataracts during the first weeks or months of life, as a result of the accumulation, in the lens, of galactitol, a product of an alternative route of galactose utilization. The development of early cataracts in homozygous affected infants is fully preventable through early diagnosis and treatment with a galactose-restricted diet. Some studies have suggested that, depending on milk consumption later in life, heterozygous carriers of galactokinase deficiency may be prone to presenile cataracts at 20–50 years of age.
Gallstone is a crystalline concretion formed within the gallbladder by accretion of bile components. These calculi are formed in the gallbladder, but may pass distally into other parts of the biliary tract such as the cystic duct, common bile duct, pancreatic duct, or the ampulla of Vater.
Presence of gallstones in the gallbladder may lead to acute cholecystitis, an inflammatory condition characterized by retention of bile in the gallbladder and often secondary infection by intestinal microorganisms, predominantly Escherichia coli and Bacteroides species. Presence of gallstones in other parts of the biliary tract can cause obstruction of the bile ducts, which can lead to serious conditions such as ascending cholangitis or pancreatitis. Either of these two conditions can be life-threatening, and are therefore considered to be medical emergencies.
Ganglioglioma is a tumour that arises from ganglion cells in the central nervous system. The term “gangliocytoma” is sometimes equated with ganglioglioma. However, it is also sometimes equated with ganglioneuroma. In this context, the glial nature of the tumor is de-emphasized. The term “gangliocytoma” is sometimes used to imply that the tumor is entirely neuronal. While Gangliogliomas are most well known as occurring in the temporal lobe of the brain, they can occur anywhere in the brain, or in the spinal cord. Gangliogliomas in the brain are often associated with seizures.
They are the second most common cause of spinal cord tumors in children. Gangliogliomas are mature ganglion cells clustered with neoplastic glial cells.
Gastric dumping syndrome, or rapid gastric emptying is a condition where ingested foods bypass the stomach too rapidly and enter the small intestine largely undigested. It happens when the upper end of the small intestine, the duodenum, expands too quickly due to the presence of hyperosmolar (substances with increased osmolarity) food from the stomach. “Early” dumping begins concurrently or immediately succeeding a meal. Symptoms of early dumping include nausea, vomiting, bloating, cramping, diarrhea, dizziness and fatigue. “Late” dumping happens 1 to 3 hours after eating. Symptoms of late dumping include weakness, sweating, and dizziness. Many people have both types. The syndrome is most often associated with gastric surgery.
Rapid loading of the small intestine with hypertonic stomach contents can lead to rapid entry of water into the intestinal lumen. Osmotic diarrhea, distension of the small bowel (leading to crampy abdominal pain), and hypovolemia can result. In addition, people with this syndrome often suffer from low blood sugar, or hypoglycemia, because the rapid “dumping” of food triggers the pancreas to release excessive amounts of insulin into the bloodstream. This type of hypoglycemia is referred to as “alimentary hypoglycemia”.
Dumping syndrome is largely avoidable by avoiding certain foods that are likely to cause it, therefore having a balanced diet is important. Treatment includes changes in eating habits and medication. People who have gastric dumping syndrome need to eat several small meals a day that are low in carbohydrates, avoiding simple sugars, and should drink liquids between meals, not with them. Fiber delays gastric emptying and reduces insulin peaks. People with severe cases take medicine such as octreotide, cholestyramine or proton pump inhibitors (such as pantoprazole) to slow their digestion. Doctors may also recommend surgery. Surgical intervention may include conversion of a Billroth II to a Roux-en Y gastrojejunostomy.
Gaucher’s disease is a genetic disease in which a fatty substance (lipid) accumulates in cells and certain organs. Gaucher’s disease is the most common of the lysosomal storage diseases. It is caused by a hereditary deficiency of the enzyme glucocerebrosidase (also known as acid β-glucosidase). The enzyme acts on a fatty substance glucocerebroside (also known as glucosylceramide). When the enzyme is defective, glucocerebroside accumulates, particularly in white blood cells (mononuclear leukocytes). Glucocerebroside can collect in the spleen, liver, kidneys, lungs, brain and bone marrow.
Symptoms may include enlarged spleen and liver, liver malfunction, skeletal disorders and bone lesions that may be painful, severe neurologic complications, swelling of lymph nodes and (occasionally) adjacent joints, distended abdomen, a brownish tint to the skin, anemia, low blood platelets and yellow fatty deposits on the white of the eye (sclera). Persons affected most seriously may also be more susceptible to infection. Some forms of Gaucher’s disease may be treated with enzyme replacement therapy.
The disease is caused by a recessive mutation in a gene located on chromosome 1 and affects both males and females. About 1 in 100 people in the United States are carriers of the most common type of Gaucher disease.
Signs and symptoms are: painless hepatomegaly and splenomegaly, the size of the spleen can be 1500-3000 ml, as opposed to the normal size of 50-200 ml; hypersplenism – the rapid and premature destruction of blood cells, leading to anemia, neutropenia and thrombocytopenia (with an increased risk of infection and bleeding)- ; neurological symptoms occur only in some types of Gaucher’s (see below) – Type II: serious convulsions, hypertonia, mental retardation, apnea – Type III: muscle twitches known as myoclonus, convulsions, dementia, ocular muscle apraxia; osteoporosis: 75% develop visible bony abnormalities due to the accumulated glucosylceramide. A deformity of the distal femur in the shape of an Erlenmeyer flask is commonly described (aseptic necrosis of the femur joint); yellowish-brown skin pigmentation.
Genu varum (also called bow-leggedness, bandiness, bandy-leg and tibia vara), is a physical deformity marked by (outward bowing) of the leg in relation to the thigh, giving the appearance of an archer’s bow. Usually medial angulation of both femur and tibia is involved. Blount’s disease is a specific form genu varum of affecting infants and adolescents.
If a child is sickly, either with rickets or suffering from any ailment that prevents the due ossification of the bones, or is improperly fed, the bowed condition may remain persistent. Thus the chief cause of this deformity is rickets. Skeletal problems, infection, and tumors can also affect the growth of the leg, sometimes giving rise to a one-sided bow-leggedness. The remaining causes are occupational, especially among jockeys, and from physical trauma, the condition being very likely to supervene after accidents involving the condyles of the femur.
In most cases persisting after childhood, there is little or no effect on the ability to walk. Due to uneven stress and wear on the knees, however, even milder manifestations can see an accelerated onset of arthritis. Those with bowlegs and a genetic predisposition for developing arthritis will likely start having arthritic symptoms around age 30.
Generally, no treatment is required for idiopathic presentation as it is a normal anatomical variant in young children. Treatment is indicated when it persists beyond 3 and a half years old. In the case of unilateral presentation or progressive worsening of the curvature, when caused by rickets, the most important thing is to treat the constitutional disease, at the same time instructing the care-giver never to place the child on its feet. In many cases this is quite sufficient in itself to effect a cure, but matters can be hastened somewhat by applying splints.
Gestational Pemphigoid or Pemphigoid Gestationis (PG) is a dermatosis of pregnancy, being an autoimmune blistering skin disease that occurs during pregnancy, typically in the second or third trimester, and/or immediately following pregnancy. It was originally called herpes gestationis because of the blistering appearance, although it is not associated with the herpes virus. PG typically starts as a blistering rash in the naval area and then spreads over the entire body. It is sometimes accompanied by raised, hot, painful welts called plaques. There have been cases where only plaques occurred. PG creates a histamine response that causes extreme relentless itching (pruritus). The cause of PG is not known, although many researchers believe that the antibodies that protect the placenta become confused and begin to increase in number. These antibodies are directed at the skin and attack the protein that binds the outer layer of skin to the body. This action causes the skin to lift up, creating blisters.
Giant cell arteritis (GCA or temporal arteritis) is an inflammatory disease of blood vessels (most commonly large and medium arteries of the head). It is a form of vasculitis.
The name (giant cell arteritis) reflects the type of inflammatory cell that is involved (as seen on biopsy). The terms “giant cell arteritis” and “temporal arteritis” are sometimes used interchangeably, because of the frequent involvement of the temporal artery. However, it can involve other large vessels (such as the aorta in “giant cell aortitis”. Giant cell arteritis of the temporal artery is referred to as “temporal arteritis,” and is also known as “Cranial arteritis” and “Horton’s disease”.
Giardiasis or beaver fever in humans is a diarrheal infection of the small intestine by a single-celled organism called Giardia lamblia. Giardiasis occurs worldwide with a prevalence of 20–30% in developing countries. In the USA, 20,000 cases are reported to the CDC annually, but the true annual incidence is estimated at 2 million people. Giardia has a wide range of mammalian hosts besides humans, thus making it very difficult to eradicate. For people with compromised immune systems, such as elderly or AIDS patients, giardiasis can be deadly.
Gigantism, also known as giantism, is a condition characterized by excessive growth and height significantly above average. This condition is caused by an over production of human growth hormone. The term is typically applied to those whose height is not just in the upper 1% of the population but several standard deviations above mean for persons of the same sex, age, and ethnic ancestry. The term is seldom applied to those who are simply “tall” or “above average” whose heights appear to be the healthy result of normal genetics and nutrition. It is usually caused by a tumor on the pituitary gland on the brain. It causes growth of the hands, face, and feet.
Many of those who have been identified with gigantism have suffered from multiple health problems involving their circulatory or skeletal system.
Gingivitis (“inflammation of the gum tissue”) is a term used to describe non-destructive periodontal disease. The most common form of gingivitis is in response to bacterial biofilms (also called plaque) adherent to tooth surfaces, termed plaque-induced gingivitis, and is the most common form of periodontal disease. In the absence of treatment, gingivitis may progress to periodontitis, which is a destructive form of periodontal disease. While in some sites or individuals, gingivitis never progresses to periodontitis, data indicates that periodontitis is always preceded by gingivitis.
The symptoms of gingivitis are somewhat non-specific and manifest in the gum tissue as the classic signs of inflammation: swollen gums; bright red or purple gums; gums that are tender or painful to the touch; bleeding gums or bleeding after brushing.
Cause of plaque-induced gingivitis is bacterial plaque, which acts to initiate the body’s host response. This, in turn, can lead to destruction of the gingival tissues, which may progress to destruction of the periodontal attachment apparatus. The plaque accumulates in the small gaps between teeth, in the gingival grooves and in areas known as plaque traps: locations that serve to accumulate and maintain plaque. Examples of plaque traps include bulky and overhanging restorative margins, claps of removable partial dentures and calculus (tartar) that forms on teeth.
Gingivitis can be prevented through regular oral hygiene that includes daily brushing and flossing. Interdental brushes are also useful in cleaning the teeth from plaque. Hydrogen peroxide, saline, alcohol or chlorhexidine mouth washes may also be employed. In a recent clinical study, the beneficial effect of hydrogen peroxide on gingivitis has been highlighted.
The focus of treatment for gingivitis is removal of the etiologic (causative) agent, plaque. Therapy is aimed at the reduction of oral bacteria, and may take the form of regular periodic visits to a dental professional together with adequate oral hygiene home care. Thus, several of the methods used in the prevention of gingivitis can also be used for the treatment of manifest gingivitis, such as scaling, root planing, curettage, mouth washes containing chlorhexidine or hydrogen peroxide, and flossing. Interdental brushes also help remove any causative agents.
Glioblastoma multiforme (GBM) is the most common and most aggressive type of primary brain tumor in humans, involving glial cells and accounting for 52% of all parenchymal brain tumor cases and 20% of all intracranial tumors. Despite being the most prevalent form of primary brain tumor, GBMs occur in only 2–3 cases per 100,000 people in Europe and North America. According to the WHO classification of the tumors of the central nervous system, the standard name for this brain tumor is “glioblastoma”. It presents two variants: giant cell glioblastoma and gliosarcoma. Glioblastomas are also an important brain tumor of the canine, and research is ongoing to use this as a model for developing treatments in humans. Treatment can involve chemotherapy, radiation, radiosurgery, corticosteroids, antiangiogenic therapy, and surgery.
Excepting the brainstem gliomas, glioblastoma has the worst prognosis of any CNS malignancy. Despite multimodality treatment consisting of open craniotomy with surgical resection of as much of the tumor as possible, followed by concurrent or sequential chemoradiotherapy, antiangiogenic therapy with bevacizumab, gamma knife radiosurgery, and symptomatic care with corticosteroids, median survival is about 14 months.
Although common symptoms of the disease include seizure, nausea and vomiting, headache, and hemiparesis, the single most prevalent symptom is a progressive memory, personality, or neurological deficit due to temporal and frontal lobe involvement. The kind of symptoms produced depends highly on the location of the tumor, more so than on its pathological properties. The tumor can start producing symptoms quickly, but occasionally is an asymptomatic condition until it reaches an enormous size.
GBM is more common in males, although the reason for this is not clear. Most glioblastoma tumors appear to be sporadic, without any genetic predisposition. No links have been found between glioblastoma and smoking, diet, cellular phones, or electromagnetic fields. Recently, evidence for a viral cause has been discovered, possibly SV40 or cytomegalovirus. There also appears to be a small link between ionizing radiation and glioblastoma. Some also believe that there may be a link between polyvinyl chloride (which is commonly used in construction) and glioblastoma. A recent link cited in the Lancet medical journal links brain cancer to lead exposure in the work place. There is an association of brain tumor incidence and malaria, suggesting that the anopheles mosquito, the carrier of malaria, might transmit a virus or other agent that could cause glioblastoma.
Glioma is a type of tumor that starts in the brain or spine. It is called a glioma because it arises from glial cells. The most common site of gliomas is the brain. Symptoms of gliomas depend on which part of the central nervous system is affected. A brain glioma can cause headaches, nausea and vomiting, seizures, and cranial nerve disorders as a result of increased intracranial pressure. A glioma of the optic nerve can cause visual loss. Spinal cord gliomas can cause pain, weakness, or numbness in the extremities. Gliomas do not metastasize by the bloodstream, but they can spread via the cerebrospinal fluid and cause “drop metastases” to the spinal cord.
Treatment for brain gliomas depends on the location, the cell type and the grade of malignancy. Often, treatment is a combined approach, using surgery, radiation therapy, and chemotherapy. The radiation therapy is in the form of external beam radiation or the stereotactic approach using radiosurgery. Spinal cord tumors can be treated by surgery and radiation. Temozolomide is a chemotherapeutic drug that is able to cross the blood-brain barrier effectively and is being used in therapy.
Glossophobia or speech anxiety is the fear of public speaking. Many people only have this fear, while others may also have social phobia or social anxiety disorder. Stage fright may be a symptom of glossophobia. Symptoms include: intense anxiety prior to, or simply at the thought of having to verbally communicate with any group; avoidance of events which focus the group’s attention on individuals in attendance; physical distress, nausea, or feelings of panic in such circumstances.
The more specific symptoms of speech anxiety can be grouped into three categories: physical, verbal, and non-verbal. Physical symptoms result from the sympathetic part of the autonomic nervous system (ANS) responding to the situation with a “fight or flight” reaction. Since the modus operandi,or method of operating, of the symphatetic system is all-or-nothing, adrenaline secretion produces a wide array of symptoms at once – all of which are supposed to enhance your ability to fight or escape a dangerous scenario. These symptoms include acute hearing, increased heart rate, increased blood pressure, dilated pupils, increased perspiration, increased oxygen intake, stiffening of neck/upper back muscles, and dry mouth. Some of these may be alleviated by drugs such as beta-blockers, which bind to the adrenalin receptors of the heart, for example. The verbal symptoms include, but are not limited to a tense voice, a quivering voice, and repetition of “Umms” and “Ahhs”—vocalized pauses—which tend to comfort anxious speakers. One form of speech anxiety is dysfunctional speech anxiety, in which the intensity of the “fight or flight” response prevents an individual from performing effectively.
Many people report stress-induced speech disorders which are only present during public speech. Some glossophobics have been able to dance, perform in public, or even to speak (such as in a play) or sing if they cannot see the audience, or if they feel that they are presenting a character or stage persona rather than themselves.
Estimated 95% of all speakers experience some degree of anxiety/nervousness when public speaking.
Gonorrhea (also colloquially known as the clap) is a common sexually transmitted infection caused by the bacterium Neisseria gonorrhoeae. The usual symptoms in men are burning with urination and penile discharge. Women, on the other hand, are asymptomatic half the time or have vaginal discharge and pelvic pain. In both men and women if gonorrhea is left untreated, it may spread locally causing epididymitis or pelvic inflammatory disease or throughout the body, affecting joints and heart valves. Treatment is commonly with ceftriaxone as antibiotic resistance has developed to many previously used medications.
Half of women with gonorrhea are asymptomatic while others have vaginal discharge, lower abdominal pain or pain with intercourse. Most men who are infected have symptoms such as urethritis associated with burning with urination and discharge from the penis. The incubation period is 2 to 30 days with most symptoms occurring between 4–6 days after being infected.
Gonorrhea if left untreated may last for weeks or months with higher risks of complications. As of 2010 injectable ceftriaxone appear to be one of the few effective antibiotics. Due to increasing rates of antibiotic resistance local susceptibility patterns need to be taken into account when deciding on treatment. Many antibiotics that where once effective including penicillin, tetracycline and fluoroquinolone are no longer recommended due to high rates of resistance.
Gout (also known as podagra when it involves the big toe) is a medical condition usually characterized by recurrent attacks of acute inflammatory arthritis—a red, tender, hot, swollen joint. The metatarsal-phalangeal joint at the base of the big toe is the most commonly affected (~50% of cases). However, it may also present as tophi, kidney stones, or urate nephropathy. It is caused by elevated levels of uric acid in the blood which crystallize and are deposited in joints, tendons, and surrounding tissues.
Diagnosis is confirmed clinically by the visualization of the characteristic crystals in joint fluid. Treatment with nonsteroidal anti-inflammatory drugs (NSAIDs), steroids, or colchicine improves symptoms. Once the acute attack has subsided, levels of uric acid are usually lowered via lifestyle changes, and in those with frequent attacks allopurinol or probenicid provide long-term prevention.
Gout has increased in frequency in recent decades affecting approximately 1–2% of the Western population at some point in their lives. The increase is believed to be due to increasing risk factors in the population, such as metabolic syndrome, longer life expectancy and changes in diet. Gout was historically known as “the disease of kings” or “rich man’s disease”.
Gout can present in a number of ways, although the most usual is a recurrent attack of acute inflammatory arthritis (a red, tender, hot, swollen joint). The metatarsal-phalangeal joint at the base of the big toe is affected most often, accounting for half of cases. Other joints, such as the heels, knees, wrists and fingers, may also be affected. Joint pain usually begins over 2–4 hours and during the night. The reason for onset at night is due to the lower body temperature then. Other symptoms that may occur along with the joint pain include fatigue and a high fever.
Hyperuricemia is the underlying cause of gout. This can occur for a number of reasons, including diet, genetic predisposition, or underexcretion of urate, the salts of uric acid. Renal underexcretion of uric acid is the primary cause of hyperuricemia in about 90% of cases, while overproduction is the cause in less than 10%. About 10% of people with hyperuricemia develop gout at some point in their lifetimes. Dietary causes account for about 12% of gout, and include a strong association with the consumption of alcohol, fructose-sweetened drinks, meat, and seafood.
Gymnophobia is a fear (phobia) of nudity. Gymnophobics experience anxiety from nudity, even if they realize their fear is irrational. They may worry about seeing others naked or being seen naked, or both. Their fear may stem from a general anxiety about sexuality, from a fear that they are physically inferior, or from a fear that their nakedness leaves them exposed and unprotected. The word “Gymnophobia” is derived from the Greek “gymnos” (naked).
Standards of modesty (also called demureness or reticence) generally prevent public nudity. Avoidance of nudity in private situations may be a continuation of modesty, or may extend to prudishness or body shame. Only an actual fear of nudity qualifies as gymnophobia. Only when the fear is beyond one’s control or is interfering with daily life can an anxiety disorder diagnosis be made.